Effect of eicosapentaenoic acid on glucose-induced diacylglycerol synthesis in cultured bovine aortic endothelial cells

Tatsuya Kuroki, Toyoshi Inoguchi, Fumio Umeda, Hajime Nawata

    研究成果: Contribution to journalArticle査読

    22 被引用数 (Scopus)

    抄録

    Hyperglycemia has been postulated to increase diacylglycerol (DAG) level through de novo synthesis pathway and subsequently activate protein kinase C (PKC) in vascular cells, possibly leading to vascular dysfunction associated with diabetes. In this study, we examined the effect of eicosapentaenoic acid (EPA) on high glucose-induced increase in DAG level in cultured aortic endothelial cells (ECs). In ECs, total DAG level was significantly increased in the cells cultured with high glucose levels (400 mg/dl) compared with the cells with normal glucose levels (100 mg/dl). The addition of EPA completely prevented high glucose-induced increase in total DAG: level. In contrast, other common fatty acids such as palmitate and oleate significantly stimulated DAG syntheisis, although arachidonate did not affect it. High glucose level significantly stimulated the incorporation of 3H-palmitate into DAG, while it did not affect the incorporation of 3H-arachidonate into DAG. The addition of EPA completely prevented the high glucose-induced increase in 3H-palmitate incorporation into DAG, while it did not affect the 3H-arachidonate incorporation. These findings suggest that EPA can prevent high glucose induced-increase in DAG level in ECs, probably by specifically inhibiting de novo synthesis at the step of acylation. EPA may be one of the candidates for clinical agents normalizing activation of DAG-PKC pathway in diabetic vascular tissues and preventing vascular complications associated with diabetes.

    本文言語英語
    ページ(範囲)473-477
    ページ数5
    ジャーナルBiochemical and Biophysical Research Communications
    247
    2
    DOI
    出版ステータス出版済み - 6 18 1998

    All Science Journal Classification (ASJC) codes

    • Biophysics
    • Biochemistry
    • Molecular Biology
    • Cell Biology

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